Chronic inflammation is a risk factor for gastric carcinogenesis after Helicobacter pylori eradication [RNA-seq]

Even after endoscopic treatment of early gastric adenocarcinoma (GAC) and eradication of Helicobacter pylori (H. pylori), some patients develop a metachronous recurrence (MR), the mechanism of which is still unknown. To elucidate the mechanism and risk factors for MR, we analyzed gene expression at multiple locations of the gastric mucosa, considering the heterogeneity of gastric mucosal damage caused by H. pylori infection and investigated the mechanism and risk factors for MR. Overall design: Five patients with MR (MR group) and five patients without MR (control) after early GAC treatment and eradication of H. pylori were included. In each case, mucosal tissue was collected as biopsy specimens from four sites in the stomach. In each patient, one specimen was obtained from the lesser curvature of the antrum (LA) and the greater curvature of the antrum (GA), both within 2-3 cm from the pylorus, middle portion of the lesser curvature of the body between the cardia and angle (LB), and middle portion of the greater curvature of the corpus (GB).mRNA sequencing and microRNA(miRNA) sequencing were performed.